Sara Jandeska | Northwestern University (Kellogg) (original) (raw)

Papers by Sara Jandeska

Ndt Plus, Oct 21, 2019

Background. Previous studies have established an association between low birthweight (LBW) and fu... more Background. Previous studies have established an association between low birthweight (LBW) and future kidney disease, but few have explored the progression of kidney dysfunction through the pediatric years leading up through adolescence and young adulthood. Methods. To better understand the temporal effects of birthweight on kidney disease progression, we conducted a retrospective cohort study comparing the glomerular filtration rate (GFR) between LBW (<2500 grams) and normal birthweight (NBW) infants who were admitted to the neonatal intensive care unit (NICU) at our institution from 1992 to 2006. Results. Age at follow-up ranged 1-26 years old. GFR was found to be significantly lower in participants born with LBW than those born with NBW, with a mean difference of 5.5 mL/min/1.73m 2 (P < 0.01). These differences were found in the adolescent and young adult age group over 9 years of age, specifically in the extremely low birthweight group (ELBW) whose birthweight was less than 1000 grams. Conclusions. We recommend screening for CKD in ELBW individuals starting at the age of 9 years old, regardless of their previous medical history.

Journal of the American Society of Nephrology

Background Genetic testing in CKD has recently been shown to have diagnostic utility with many pr... more Background Genetic testing in CKD has recently been shown to have diagnostic utility with many predicted implications for clinical management, but its effect on management has not been prospectively evaluated. Methods Renasight Clinical Application, Review, and Evaluation RenaCARE (ClinicalTrials.gov NCT05846113) is a single-arm, interventional, prospective, multicenter study that evaluated the utility of genetic testing with a broad, 385 gene panel (the RenasightTM test) on the diagnosis and management of adult patients with CKD recruited from 31 US-based community and academic medical centers. Patient medical history and clinical CKD diagnosis were collected at enrollment. Physician responses to questionnaires regarding patient disease categorization and management were collected before genetic testing and 1 month after the return of test results. Changes in CKD diagnosis and management after genetic testing were assessed. Results Of 1623 patients with CKD in 13 predefined clinica...

Pediatrics

A 10-year-old male with a past medical history of premature pubarche, mild persistent asthma, and... more A 10-year-old male with a past medical history of premature pubarche, mild persistent asthma, and eczema presented to the emergency department with progressive dyspnea and chest pain. On examination, he was found to be tachycardic and tachypneic. Chest radiograph demonstrated cardiomegaly, bilateral pleural effusions, and scattered atelectasis. Echocardiogram revealed a large pericardial effusion with right atrial collapse. The patient was admitted to the pediatric ICU for pericardiocentesis and drain placement. As he later became hypertensive and febrile, we will discuss how our patient’s hospital course guided our differential diagnosis and how we arrived at a definitive diagnosis using a multidisciplinary approach.

Blood, 1998

Interferon-alpha (IFNα) mediates its biological effects through activation of the JAK-STAT signal... more Interferon-alpha (IFNα) mediates its biological effects through activation of the JAK-STAT signaling pathway and it has been shown to be one of most effective therapeutic agents for a number of hematological malignancies, including cutaneous T-cell lymphoma (CTCL). Nevertheless, its efficacy is limited by the development of clinical resistance but the reasons for resistance in CTCL are unknown. Here, we report the development of an IFNα-resistant CTCL cell line (HUT78R), characterized by its ability to proliferate in high concentration of recombinant IFNα, which can be used as a model system to study IFN resistance. The levels of IFN receptor expression and binding affinity were found to be comparable between the parental sensitive (HUT78S) and resistant (HUT78R) cells. However, IFNα stimulation failed to induce interferon-stimulated gene factor 3 (ISGF3) complex formation in HUT78R cells. In addition, the expression of the IFN-inducible 2-5 OAS gene was significantly reduced in HUT...

Clinical Kidney Journal, 2019

Background Previous studies have established an association between low birthweight (LBW) and fut... more Background Previous studies have established an association between low birthweight (LBW) and future kidney disease, but few have explored the progression of kidney dysfunction through the pediatric years leading up through adolescence and young adulthood. Methods To better understand the temporal effects of birthweight on kidney disease progression, we conducted a retrospective cohort study comparing the glomerular filtration rate (GFR) between LBW…

Pediatric Transplantation, 2017

Antibody-mediated rejection leads to allograft loss after kidney transplantation. Bortezomib has ... more Antibody-mediated rejection leads to allograft loss after kidney transplantation. Bortezomib has been used in adults for the reversal of antibody-mediated rejection; however, pediatric data are limited. This retrospective study was conducted in collaboration with the Midwest Pediatric Nephrology Consortium. Pediatric kidney transplant recipients who received bortezomib for biopsy-proven antibody-mediated rejection between 2008 and 2015 were included. The objective was to characterize the use of bortezomib in pediatric kidney transplant recipients. Thirty-three patients received bortezomib for antibody-mediated rejection at nine pediatric kidney transplant centers. Ninety percent of patients received intravenous immunoglobulin, 78% received plasmapheresis, and 78% received rituximab. After a median follow-up of 15 months, 65% of patients had a functioning graft. The estimated glomerular filtration rate improved or stabilized in 61% and 36% of patients at 3 and 12 months post-bortezomib, respectively. The estimated glomerular filtration rate at diagnosis significantly predicted estimated glomerular filtration rate at 12 months after adjusting for chronic histologic changes (P .001). Fifty-six percent of patients showed an at least 25% reduction in the mean fluorescence intensity of the immune-dominant donor-specific antibody, 1-3 months after the first dose of bortezomib. Non-life-threatening side effects were documented in 21 of 33 patients. Pediatric kidney transplant recipients tolerated bortezomib without life-threatening side effects. Bortezomib may stabilize estimated glomerular filtration rate for 3-6 months in pediatric kidney transplant recipients with antibody-mediated rejection.

Human Immunology, 2017

Focal Segmental Glomerulosclerosis (FSGS) can lead to ESRD requiring a renal transplant and the r... more Focal Segmental Glomerulosclerosis (FSGS) can lead to ESRD requiring a renal transplant and the rate of recurrent FSGR (rFSGS) is high. The exact mechanisms of the pathogenesis of FSGS and rFSGS is unclear and both FSGS and rFSGS have similar pathological findings and clinical symptoms. To date there are no good tests that can predict FSGS or rFSGS. A very recent report indicated that antibodies against Angiotensin Receptor Type 1 (AT1R-Ab) could predict rFSGS post-transplant. Angiotensin II (AT II) acts on angiotensin 1 receptor (AT1R) and exerts hemodynamically vital actions. AT1Rs are extensively distributed across various organ systems including renal podocytes. Over-activation of AT1R via AT II or AT1R-Ab could trigger events leading to chronic renal injury. Presence of AT1R-Ab was shown to be associated with vascular rejection and malignant hypertension in the absence of detectable allograft-specific HLA antibodies and also in C4d positive AMR in a zero mismatch (ABDR) renal transplant in the absence of HLA DSAs. We present a case of a 7 year old African American male with biopsy-proven FSGS and typical features of nephrotic syndrome including proteinuria of 13 g/g based on protein to creatinine ratio. Upon initial diagnosis he was treated with steroids. Cessation of the steroids resulted in recurrence of his nephrotic syndrome. Additionally he was diagnosed with hypertension (HTN) and left ventricular hypertrophy both treated with an ACE inhibitor. He unfortunately progressed in terms of his chronic kidney disease to ESRD requiring a cadaveric renal transplant, performed in Jan 2016. His mean AT1 -Ab levels were 266.18 ± 36.06 (n = 7) and 120.72 ± 37.53 U/ML (n = 5) pre and post-transplant respectively (>17 units of AT1R-Ab is considered positive). Currently the patient is doing well on maintenance immunosuppression without recurrence of his original disease. The practice of screening for AT1R-Ab in pre and post renal transplant patients is gradually evolving. Considering the mechanisms of AT1R activation and subsequent downstream events, early monitoring for AT1R antibody levels in similar patients with HTN and idiopathic FSGS may help in appropriate management of preventing multi-organ injuries, malignant HTN, metabolic disorders and eventual ESRD. More patients with pre-transplant FSGS and r FSGS post transplant need to be evaluated for AT1R-Ab.

Frontiers in Bioscience, 2009

Introduction 3. TGF-beta and the pathogenesis of kidney disease 4. The canonical TGF-beta signali... more Introduction 3. TGF-beta and the pathogenesis of kidney disease 4. The canonical TGF-beta signaling pathway 5. Regulation of TGF-beta expression and activity 6. Regulation of TGF-beta signaling 6.1. Regulation of at the level of the receptor 6.2. Smad expression 6.3. Post-translational modification of Smads 6.4. Adaptor molecules 6.5. Regulation of transcriptional activity 6.5.1. Enhancers 6.5.2. Inhibitors 6.6. Cross-talk with other signaling pathways 7. Interaction of TGF-beta signaling with other growth factors/hormonal mediators 7.1. Bone morphogenetic protein 7.2. Hepatocyte growth factor 7.3. Glucose and angiotensin II 7.4. Connective tissue growth factor 7.5. Nuclear receptor-associated hormones 8. Regulation of tissue functions in the kidney 8.1. The podocyte and the glomerular filtration barrier 8.2. Hyperplasia and hypertrophy 8.3. Epithelial-to-mesenchymal transition 9. Perspective 10. Acknowledgments 11. References

Transplantation Proceedings, 1997

Journal of Pediatric Hematology/Oncology